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Clinical Flashcards

1
Q

What is osteoarthiritis?

A

Articular cartilage thinning or loss

commonly called “wear & tear” in the joints

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2
Q

what are the risk factors for osteoarthritis?

A 
Age
male sex
Obesity
Previous injury
Occupation
Sports activities
Muscle weakness
Proprioceptive deficits
Genetic elements
Acromegaly
Joint inflammation
Crystal deposition in cartilage
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3
Q

What are the two main types of OA?

A

Primary/idiopathic

Secondary

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4
Q

what are the main causes of secondary OA?

A

Joint disease

Haemochromatosis

Obesity

Calcium crystal deposition disease

occupational related

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5
Q

What are the main sites of OA?

A

Knees or Hip are Main ones

others:

spine ( cervical or lumbar)

HAND (DIP,PIP, 1st IP, 1st MCP, CMC)

FOOT ( MTP joint)

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6
Q

What are the signs and symptoms of OA?

A
  1. Localised disease ( often knee and hip):

Pain and creptius on movement. Made worse on prolonged activity

Stiffness

joint effusion

restriction of movement

Hip pain - Pain may be felt in groin or radiating to knee

  1. Generalised disease : Nodal OA (typically hand joints)

Tenderness

derangement and bone swelling

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7
Q

How do you diagnose OA?

A

1.Radiography shows:

Loss of joint space
Osteophytes
Subarticular sclerosis
Subchondral cysts

2.Kellgren-Lawrence Radiographic Grading Scale of Osteoarthritis:

Grade 0-No radiographic findings of osteoarthritis

Grade 1- Minute osteophytes of doubtful clinical significance

Grade 2 - Definite osteophytes with unimpaired joint space

Grade 3 - Definite osteophytes with moderate joint space narrowing

Grade 4 - Definite osteophytes with severe joint space narrowing and subchondral sclerosis

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8
Q

How do you manage OA?

A

Exercise to improve local muscle strength and general aerobic fitness

weight loss if overweight

Pharmacological:

  1. Analgesia - Paracetamol +/- topical NSAIDs
  2. If Paracetamol and topical NSAID are ineffective then add oral NSAID/COX-2 inhibitor to paracetamol should be considered. Use PPI for either
  3. Intra-articular steroid injections for temporary relief if there are severe symptoms

Surgery:

  1. Joint replacements
  2. Arthroscopic washout, Loose body, soft tissue trimming.
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9
Q

What is gout?

A

Inflammation in the joint triggered by uric acid crystals

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10
Q

what are the main causes and risk factors for gout?

A

Deposition of monosodium urate crystals in and near joints

  1. Reduced Urate excretion: Elderly, men, post-menopausal women, impaired renal function, hypertension, aspirin and Diuretics
  2. Excess urate production: Dietary (alcohol, sweeteners and seafood/red meat), genetic disorders, Myeloproliferative/Lymphoproliferative disorders and psoraisis
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11
Q

What are the most common sites effected by gout?

A
  1. Metatarsophalangeal joint of the big toe

2. Ankle, foot, small joints of the hand, wrist, elbow or knee

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12
Q

What are the signs and symptom of Gout?

A

Acute monoarthropathy with severe joint inflammation

Acute Gout:

Settles in about 10 days without treatment
Settles in about 3 days with treatment
Abrupt onset, often overnight
May have normal uric acid during acute attack

Chronic gout:
Chronic joint inflammation 
Often diuretic associated
High serum uric acid
Tophi
May get acute attacks
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13
Q

How do you diagnose Gout?

A
  1. Needle-shaped monosodium urate crystals found in negative birefringence under polarised light in synovial fluid
  2. Serum Urate (SUA) raised. Might be normal in acute attack
  3. Inflammatory markers
  4. punched out erosions in juxta-articular bone
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14
Q

How do you manage Gout?

A

1.Acute gout:

High-dose NSAID if contraindication use Colchicine which is slower

  1. Prevention: lose weight, avoid prolonged fasts, avoid purine rich meats and avoid low dose aspirin
  2. Prophylaxis e.g. allopurinol or Febuxostat
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15
Q

What is Calcium pyrophosphate deposition (CPPD)?

A

two types:

  1. Calcium pyrophosphate
  2. Calcium hydroxy appatite crystals (pseudogout)
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16
Q

What are the risk factors of CPPD?

A

Elderly

usually spontaneous but can be provoked by illness, surgery or trauma

hyperparathyroidisim

Haemochromatosis

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17
Q

What are the signs and symptoms of CPPD?

A

Acute monoarthropathy usually of larger joints in elderly

Chronic CPPD inflammatory RA like (symmetrical) polyarthritis and synovitis

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18
Q

How do you diagnose CPPD?

A

Needle-shaped monosodium urate crystals found in positivie birefringence under polarised light in synovial fluid

associated with soft tissue calcium deposition on X-ray

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19
Q

How do you manage CPPD?

A

Acute Attacks: cool packs, rest, aspiration and intra-articular steroids. NSAIDs (+PPI)

Methotrexate or hydroxychloroquine for chronic CPP inflammatory arthritis

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20
Q

what is Hydroxyapatite?

A

Hydroxyapatite crystal deposition in or around the joint. There is acute and rapid deterioration

commonly in the shoulder joint

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21
Q

How do you diagnose Hydroxyapatite?

ii. what is the main epidemiology?

A

Release of collagenases, serine proteinases and IL-1

ii. Females, 50-60 years

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22
Q

How do you manage Hydroxyapatite?

A

NSAIDs

Intra-articular steroid injection

Physiotherapy

Partial or total arthroplasty

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23
Q

What is the modified Beighton score?

A

> 10º hyperextension of the elbows

Passively touch the forearm with the thumb, while flexing the wrist.

Passive extension of the fingers or a 90º or more extension of the fifth finger

Knees hyperextension ≥ 10º)

Touching the floor with the palms of the hands when reaching down without bending the knees.

Hypermobility if ≥ 4/9

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24
Q

What is soft tissue rheumatism?

A

pain that is caused by inflammation/damage to ligaments, tendons, muscles or nerve near a joint rather than either the bone or cartilage

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25
Q

What is the most common areas for soft tissue rheumatism?

A

Shoulder

e.g. Adhesive Capsulitis
Rotator cuff tendinosis
Calcific tendonitis
Impingement 
Partial rotator cuff tears
Full rotator cuff tears
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26
Q

How do you diagnose and manage Soft tissue rheumatism?

A 
1.Diagnose
Tests are usually unnecessary
X-ray - calcific tendonitis
MRI if fails to settle
Identify precipitating factors
2.management
Pain control
Rest and Ice compressions
PT
Steroid injections
Surgery
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27
Q

what is vasculitis?

A

it is inflammation of the blood vessels

presentation depends on the organs involved

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28
Q

What is difference between primary and secondary vasculitis?

A

primary - results from an inflammatory response that has no known cause or is autoimmune

secondary- inflammation of the blood vessels caused by a known cause

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29
Q

What are the main causes of secondary vasculitis?

A

SLE

Rheumatoid arthritis

Hep B&C

HIV

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30
Q

What is the pathophysiology of vasculitis?

A
  1. Activated dendrite cells express receptors and release inflammatory cytokines that promote activation of T cells and vascular inflammation.
  2. Activated T cells promotes inflammation, granuloma formation and macrophage activation and differentiation
  3. Activated macrophages produce a variety of mediators that lead to progressive vascular inflammation, endothelial damage, disruption of the internal elastic lamina, and intimal hyperplasia.
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31
Q

How do you classify vasculitis?

A

Via size of blood vessel:

Large vessel: Giant cell arteritis and takayasu arteritis

Medium-vessel: Polyarteritis nodosa, kawasaki disease

small-vessel: split into two groups ANCA-associated and immune complex

ANCA-associated: Microscopic polyangitis, Granulomatosis with polyangitis ( wegener) and Eosinophilic granulomatosis with polyangitisis (churg-strauss)

Immune complex: Goodpasture’s disease, IgA vasculitis ( Henoch-schonlein)

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32
Q

What are the signs and symptoms of Vasculitis?

A

Depends on the type of which vessels affected

Systemic symptoms: Fever, malaise , weight loss, arthlagia and myalgia

Skin: Purpura, ulcers, liverdo reticularis, nail bed infarcts

Eyes: scleritis, visual loss

ENT: Epistaxis, nasal crushing , stridor , deafness, sinusitis or mouth ulcers

Pulmonary: Haemoptysis , dyspnoea and caviating nodules on CXR

Cardiac: Angina or MI, heart failure and pericarditis

GI: pain or perfoartion

Neurological: Stroke, fits, chorea, psychosis, confusion

Renal: Hypertension, haematuria, proteinuria, casts and renal failure

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33
Q

How do you diagnose Vasculitis?

A

MR angiogram or PET CT

Temporal artery biopsy - remember “skip lesions” occur so biopsy may be negative

ESR/CRP increase

ANCA may be positive - use immunofluorescence

Creatine levels increase if renal failure

urine: proteinuria, haematuria - urinanalysis

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34
Q

How do you manage Vasculitis?

A

Large- vessel:

  1. Prednisolone
  2. Steroid sparing agents may be considered

Medium/small vessel:

  1. immunosuppression ( steroids +/- another agents)
    e. g. Cyclophosamide if severe or methotrexate/azathioprine
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35
Q

What is Henoch-schlonlein purpura ( HSP)?

A

Henoch-Schönlein purpura (HSP) affects the blood vessels and causes a spotty rash

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36
Q

What is the main cause of HSP?

A

group A streptococcus

mainly preceded by URTI, Pharyngeal infection or GI infection

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37
Q

What are the signs and symptoms of HSP?

A

Purpuric rash typically over buttocks and lower limbs

colicky abdominal pain

bloody diarrhoea

Joint pain ( may have sweeling)

Renal involvement issues ( 50% of patients)

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38
Q

How do you manage HSP?

A

usually self- limiting

symptoms tend to resolve within 8 weeks but relapse can occur

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39
Q

Which types of Vasculitis are positive for cANCA?

A

Granulomatosis with Polyangitis (GPA)

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40
Q

which types of vasculitis are positive for pANCA?

A

EGPA - eosinophilic granulomatosis with polyangitis

Microscopic Polyangitis (MPO)

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41
Q

What is Giant cell arteritis/ temporal arteritis?

A

form of vasculitis common in the elderly (over 55)

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42
Q

what are the signs and symptoms of GCA?

A

Headache

temporal artery

scalp tenderness

tongue/jaw claudication

amaurosis fugax - loss of eyesight in one or two eyes due to lack of blood flow

Extracranial symptoms: malaise, dyspnoea, weight loss, morning stiffness

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43
Q

How do you diagnose GCA?

A

Huge rise in ESR/CRP

Platelet increase

ALP increase

Hb decrease

temporal artery biopsy- skip lesions do occur so may be negative

PET scan

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44
Q

How do you manage GCA?

A

Prednisolone immediately or IV methylprednisolone if evolving visual loss or history of amaurosis fugax

Give PPI, Biphosphate, calcium with coleciferol and aspirin

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45
Q

what is polyarteritis nodosa (PAN)?

A

necrotising vasculitis that causes aneurysms and thrombosis, leading to infarction in affected organs with severe systemic symptoms

more common in men

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46
Q

Which organs are least associated with PAN?

A

Lungs

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47
Q

what is microscopic polyangititis? (MPO)

A

Necrotising vasculitis affecting small and medium sized vessels.

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48
Q

What are the signs and symptoms of MPO?

A

rapidly progressive glomerulonephritis

and pulmonary haemorrhoages are common

plus normal symptoms of vasculitis

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49
Q

What is Rheumatoid arthritis?

A

Chronic systemic inflammatory disease, characterised by a symmetrical, deforming, peripheral polyarthritis

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50
Q

What is the epidemiology RA?

A

women 3 times more likely than men

can affect any age group - most common starts at 50s/60s

prevalence is 1%

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51
Q

What is the pathogenesis of RA?

A

main triggers are smoking and infections

severity based upon genetic factors and presence of auto- antibodies

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52
Q

What are the main sites affected by RA?

A

Synovium structures of joints most affected

small joints in hands and feet most common. However large joints may be involved

writsts, elbows,shoulders, knees, hips and ankles are also examples of joints affected

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53
Q

what are the signs and symptoms of RA?

A

symmetrical swollen, painful stiff small joints of hands and feet (PIPs/MCPs and MTPs)

prolonged morning stiffness

  1. less common presentations: sudden onset, widespread arthritis

systemic illness may occur: e.g. fatigue, malaise and weight loss

  1. later signs of RA: Joint damage/deformity, Ulnar deviation and subluxation of the wrist and fingers or Z-deformity of thumbs occur.
  2. Extra-articular mainfestations: Nodule found on elbows, lungs (ILD, bronchiectasis , pulmonary fibrosis and PE), cardiac, CNS and vasculitis

Lung: pleural disease, interstitial fibrosis

Cardiac: IHD, Pericarditis, perifardial effusion

Eye: Scleritis, episcleritis and keratoconjunctivitis

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54
Q

How do you diagnose RA?

A

1.auto antibodies
Rheumatoid factor: Sensitivity 50-80%
Specificity 70-80%

Antibodies to cyclic citrullinated peptide (Anti-CCP antibodies):
Sensitivity 60-70%
Specificity 90-99%

  1. ESR/CRP increase and platelet levels rise
  2. Imaging:

X-rays:

Early disease:
Normal
Soft tissue swelling
Periarticular osteopenia.

Late disease:
Erosions
Subluxation

US:
Increased sensitivity for synovitis in early disease
Consistently superior to clinical examination
Can detect more MCP erosions than plain x-ray in early RA
Useful in making treatment changes

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55
Q

How do you manage RA?

A
  1. Disease activity measured using 28-joint disease activity score
  2. Give early use of Disease modifying anti-rheumatic drugs (DMARDS) e.g. Methotrexate 1st choice, Sulfasalazine, Leflunomide, Hydroxychloroquine mainly for lupus and steroids
  3. Steroids rapidly reduce symptoms and inflammation.
  4. NSAIDS for symptom relief but no effect on disease
  5. Biologics: give when Tried 2 DMARDs
    DAS 28 score >5.1
e.g. Anti TNF agents- Infliximab, Etanercept, Adalimumab.
T cell receptor blocker-Abatacept.
B cell depletor-Rituximab
IL-6 blocker-Tocilizumab.
JAK inhibitors-Tofacitinib, Baricitinib
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56
Q

what are the side effects of DMARDs?

A 
Bone marrow suppression
Infection
Liver function derangement
Pneumonitis 
Nausea
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57
Q

What is systemic lupus erythematosus (SLE)?

A

Multisystemic autoimmune disease. Auto-antibodies are made against a variety of autoantigens which form immune complexes

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58
Q

What is the epidemiology of SLE?

A
  1. 2% of population
    9: 1 women:men

commoner in Afro-Caribbean, Asians and Hispanic-Americans

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59
Q

What is the pathogenesis of SLE?

A
  1. Loss of immune regulation
  2. increased and defective apoptosis
  3. Necrotic cells release nuclear materials which act as auto-antigens
  4. Auto-immunity results from exposure to nuclear and cellular auto-antigens
  5. B and T cells are stimulated
  6. Auto-antibodies are produced
  7. Complexes of antigens and auto-anbodies form and circulate
  8. deposition of immune complexes in basement membrane
  9. cytokine release perpetuates inflammation which causes necrosis and scarring
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60
Q

What are the signs and symptoms of SLE?

A

SLE mimics other illnesses

EULAR/ACR 2019 SLE classification criteria:

  1. ANA must be positive
  2. Score >10

Clinical criteria:

  1. Constitiutional domain: fever, malaise, myagia and fatigue
  2. Cutaneous domain:
    Nonscarring alopecia, oral ulcers, subacute cutaneous lupus (Malar rash), Chronic cutanoeus lupus (discoid rash)
  3. Arthritis domain: Synovitis
  4. Neurologic domain: delirium, psychosis, seizure
  5. Serositis domain: pleural or pericardial effusion, acute pericarditis
  6. Haematoligical domain: leukopenia, thrombocytopenia and autoimmune haemolysis
  7. renal domain: proteinuria >0.5g/24hr, class II lupus nephritis, class III lupus nephritis
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61
Q

What is the difference between malar rash and discoid rash?

A

Malar rash - red fixed erythema rash ,flat or raised over the malar eminences. spares the nose

Diiscoid rash - red/white rash erythematous raised patches with adherent keratotoic scales. three staged rash

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62
Q

What are the immune criteria for SLE?

A
  1. +ve ANA ( positive in 95% of cases)
  2. Anti- dsDNA - highly specific ( only in 60% of cases)
  3. Anti-smooth antibodies present
  4. Antiphospholipid antibodies present
  5. Low C3 and/or C4
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63
Q

How do you diagnose SLE?

A

Mainly through criteria

when monitoring three best tests:

  1. Anti-dsDNA antibody titres
  2. Complement proteins
  3. ESR
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64
Q

How do you manage SLE?

A

general: Sun protection, vaccinations, exercise, no smoking, lose weight, monitor blood pressure, lipids and glucose
1. Mild

1st line: Hydroxychloroquine, Glucorticosteroids oral/intramuscular

refractory: Hydroxychloroquine, Glucorticosteroids oral/intramuscular and Methotrexate/azathioprine
2. Moderate

1st line: Hydroxychloroquine, Glucorticosteroids oral/intramuscular and Methotrexate/azathioprine,, calcineurin inhibitors and cyclophosphamide

Refractory: Hydroxychloroquine, Glucorticosteroids oral/intramuscular and Methotrexate/azathioprine,, calcineurin inhibitors , mycophenolate mofeti and belimumab

  1. Severe

1st line: Hydroxychloroquine, Glucorticosteroids oral/intramuscular, cyclophosphamide and mycophenolate mofeti

refractory: Hydroxychloroquine, Glucorticosteroids oral/intramuscular, cyclophosphamide and rituximab

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65
Q

What is Sjogren’s syndrome?

A

A chronic inflammatory autoimmune disorder. Which can be primary or secondary.

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66
Q

what is the epidemiology of Sjorgren’s syndrome?

A

(9:1 women:men) onset 4th- 5th decade

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67
Q

What are the signs and symptoms of Sjorgren’s symptom?

A

Dry eyes and kertoconjunvitivis - decrease in tear production

Dry mouth (xerostomia) - decrease in saliva production

Dry throat

Vaginal dryness

Bilateral parotid gland swelling

Joint pain

fatigue

Unexplained increase in dental caries

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68
Q

How do you diagnose Sjorgren’s?

A

Schrimer’s test measure conjunctival dryness

Immunology: anti-Ro and Anti-La (26% and 40%)

ANA is usually +ve

RF can be +ve (40% of cases)

May have raised IgG and raised ESR

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69
Q

What does Sjogren increase the risk of?

A

Lymphoma

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70
Q

What is systemic sclerosis?

A

Is a multisystem autoimmune disease which features scleroderma (Skin fibrosis), internal organ fibrosis and mircrovascular abnormalities

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71
Q

What are the signs and symptoms of Systemic sclerosis?

A

Raynaud’s syndrome

Skin thickening

Difficulty swallowing

GORD

telangiectasia- widened venules cause threadlike red lines or patterns on the skin

calcinosis

may have SOB

Two types of SLE

  1. Diffuse: Skin involvement on extremities above & below elbows and knees ( plus face and trunk). i.e. whole body
  2. Limited: Face hand and feet. i.e. rule is below elbows and knees (plus face). associated with pulmonary hypertension
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72
Q

what antibodies are assoicated with limited systemic sclerosis?

A

Anticentromere antibodies

Anti-To/Th

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73
Q

What antibodies are associated with diffuse systemic scleorsis?

A

Anti-topoisonmerase-1 antibodies

anti-RNA polymerase

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74
Q

what are the main GI complications associated with systemic sclerosis?

A
  1. Dysphagia
  2. GORD
  3. Watermelon stomach
  4. Small intestinal bacterial overgrowth
  5. Malabsorption
  6. Fluctuating bowel habit
  7. Faecal incontinence
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75
Q

What are the main cardio and resp complications associated with Systemic scleorsis?

A
  1. Interstitial lung disease
  2. Pulmonary arterial hypertension
  3. Myocardial disease
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76
Q

What are the main renal complications associated with systemic sclerosis?

A

Scleroderma renal crisis

Non specific progessive renal dysfunction

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77
Q

What are the three main clinical features of Raynaud’s phenomemen?

A

best seen on hands

  1. Blanching - white
  2. Acricyanosis - purple
  3. Reactive hyperaemia- redness
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78
Q

How do you manage systemic sclerosis?

A

No cure

  1. Management of Raynaud’s

CCBs ( nifedipine usually first line treatment)

ARBs and nitrates

PDE-5 inhibitor ( e.g. sildenafil)

Prostacyclin infusion (e.g. iloprost)

Endothelin receptor antagonist (e.g. Bosentan)

  1. Management of Pulmonary hypertension

screen every year

use immunosupression:

Myophenolate mofetil

Rarely cyclophosphamide ( for very aggressive disease)

Rixtuximab as a second line agent

Nintedanib- antifibrotic

  1. Management of renal disease

Regular ACE or ARBS decrease risk of renal issue

monitor BP and renal function

  1. Management of skin fibrosis

methotrexate and mycophenolate

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79
Q

Give examples of causes for “mechanical” back pain.

A
  1. Obesity
  2. poor posture
  3. Poor lifting technique
  4. Lack of physical activity
  5. Depression
  6. Degenerative disc prolapse
  7. Facet Joint OA
  8. Spondylosis
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80
Q

What is spondylosis?

A

Where the intervertebral discs lose water content with age resulting in less cushioning and increased pressure on the facet joints leading to secondary OA

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81
Q

How do you manage “mechanical” back pain?

A

Analgesia

physiotherapy

reassure patents that it is not a serious problem

do not advise bed rest - lead to stiffness and spasm

spinal stabilisation surgery - if patient hasn’t improved from physiotherapy and is affected by OA or instability

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82
Q

How can an acute disc tear occur?

A

Occurs in the outer annulus fibrosis of an intervertebral disc which normally happens after lifting a heavy object

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83
Q

What are the symptoms of an acute disc tear?

A

severe back pain

made worse on coughing - increases disc pressure

symptoms resolve after 2-3 months after

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84
Q

How do you manage an acute disc tear?

A

Analgesia and physiotherapy

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85
Q

What is spinal stenosis?

A

when the cauda equina of the lumbar spine has less space causes multiple nerve roots to become compressed

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86
Q

Give examples of causes for spinal stenosis.

A

Spondylosis

bulging discs

bulging ligamentum flavum

osteophytosis

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87
Q

What is the main clinical features of spinal stenosis?

A

patients usually over 60

Claudication- different to PVD claudication:

  1. Claudication distance is inconsistent
  2. Pain is burning rather than cramping like in PVD
  3. Pain is less walking uphill but worse walking downhill
  4. Pedal pulses are preserved
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88
Q

How do you diagnose spinal stenosis?

A

MRI

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89
Q

How do you manage spinal stenosis?

A

Conservative management ( analgesia, physiotherapy and weight loss)

If MRI shows stenosis then surgery can help to increase space for cauda equina

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90
Q

What is cauda equina syndrome?

A

When a very large central disc prolapse compress all the nerve roots of the cauda equina

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91
Q

What are the sign and symptoms of cauda equina?

A

Bilateral leg pain symptoms and altered bladder/bowel function is cauda equina syndrome until proven otherwise

Bilateral leg pain

Paraesthesiae or numbness.

Numbing common around the sitting area and perineum (saddle anaesthesia)

urinary retention and faecal inconteninence can occur

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92
Q

How do you diagnose cauda equina syndrome?

A
  1. PR examination - mandatory

2. urgent MRI

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93
Q

How do you manage Cauda equina syndrome?

A

urgent Discetomy

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94
Q

Give examples of Red flag symptoms for Back pain.

A
  1. Back pain in the younger patients <20 - children more susceptible to infection.
  2. New back pain in the older patients <60 - higher risk of arthritic change, crush fracture or malignancy
  3. Nature of pain : constant severe pain which is worse at night - Tumour and infection main cause of this complaint
  4. Sytemic upset : fevers, night sweats, weight loss, fatigue and malaise - may indicate tumour or infection
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95
Q

What can osteoporotic crush fracture lead to?

A

acute pain and kyphosis

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96
Q

How do you manage osteoporotic crush fractures?

A

Conservative management

balloon vertebroplasty for patients with chronic pain is being tested

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97
Q

What is the main difference between cervical nerve root compression and peripheral nerve compression?

A

Peripheral nerve compression neuropathies will cause symptoms and signs affecting peripheral nerve sensory and motor territories rather than dermatomal and myotomal distributions

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98
Q

Which nerve passes through the carpal tunnel?

A

median nerve along with 9 flexor tendons

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99
Q

What are main causes of carpal tunnel syndrome?

A

anything which causes swelling or compression of the tunnel

  1. Idiopathic
  2. secondary
    i. Pregnancy - symptoms subside after childbirth
    ii. diabetes
    iii. chronic renal failure
    iv. hypothyroidism (myoxderma)
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100
Q

which gender is more likely to suffer from carpal tunnel syndrome?

A

Women - narrower wrists but have similar sized tendons to men

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101
Q

What are the signs and symptoms of carpal tunnel syndrome?

A
  1. Aching pain in the hand and arm at night

2. Paraesthesiae in thumb, index and middle fingers -relieved by dangling the hand over the edge of the bed.

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102
Q

How do you diagnose Carpal tunnel syndrome?

A

Tinel’s test - percussing over the median nerve

Phalen’s test - holding the wrists hyper-flexed

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103
Q

How do you manage Carpal tunnel syndrome?

A

Wrist splinting - prevents flexion at night

local steroid injection

surgery: decompression surgery

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104
Q

What is cubital tunnel syndrome?

A

compression of the ulnar nerve at the elbow behind the medial epicondyle (funny bone)

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105
Q

What are the clinical features of the cubital tunnel syndrome?

A

Paraesthesiae in the ulnar 1.5 fingers

tinels test - over the cubital tunnel is usually positive

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106
Q

Define spondyloarthropathies.

A

Family of inflammatory arthritides characterised by involvement of both the spine and joints, principally in genetically predisposed (HLA B27) individuals

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107
Q

What are the main conditions associated with the HLA B27 gene?

A
  1. Ankylosing spondylitis
  2. Reactive arthritis
  3. Crohn’s disease
  4. Uveitis
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108
Q

What is the difference between Mechanical and inflammatory back pain?

A

mechanical - worsened by activity, typically worst at end of day, better with rest

Inflammatory - worse, with rest, better with activity, significant early morning stiffness. (>30 mins)

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109
Q

What are the main clinical features which spondyloarthropathies?

A
  1. Seronegativity ( Rf -ve)
  2. HLA B27 associations
  3. Axial arthritis- pathology in spine and sacroiliac joints
  4. Asymmetrical large-joint oligoarthritis or monoarthritis
  5. Enthesitis - inflammation of the site of insertion of tendon or ligament into bone
  6. Dactylitis: inflammation of an entire digit, due to soft tissue oedema
  7. Extra- articular mainfestations
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110
Q

What is Ankylosing spondylitis (AS)?

A

A chronic inflammatory disease of the spine and sacroilliac joint

more common in men who present earlier (<30 y.o)

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111
Q

What are the signs and symptoms of AS?

A
  1. Gradual onset of lower back pain
  2. worse during night with spinal morning stiffness relieved by exercise
  3. Peripheral arthritis ( shoulders and hips) - rare
  4. enthesitis ( especially achilles tendonitis, plantar fascitis at the tibial and ischial tuberosities)
  5. Progressive loss of spinal movement ( all direction) - hence decrease in thoracic expansion

Extra articular features:

  1. Anterior Uveitis
  2. Cardiovascular involvement (aortic valve)
  3. Pulmonary involvement ( fibrosis upper lobes - apical fibrosis)
  4. Asymptomatic enteric mucosal inflammation
  5. Neurological involvement
    ( rarely A-A subluxation)
  6. Amyloidosis
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112
Q

How do you diagnose AS?

A

Modified New York criteria for diagnosing of Ankylosing spondylitis (1992)

  1. limited lumbar motion
  2. Lower back pain for three months - improved with exercise not rest
  3. Reduced chest expansion
  4. Bilateral sacroilitis on X-ray (grade 2-4)
    or
  5. Unilateral sacrolilits on X ray (grade 3-4)
  6. MRI allows detection of active inflammation (bone marrow oedema) and enthesitis
  7. X-rays show Sacroilitis, syndesmophytes ( bony growth originating inside a ligament) and bamboo spine
  8. Bloods - Rise in ESR, CRP and HLA B27 +ve
  9. Schober test
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113
Q

How do you manage AS?

A

Exercise, not rest for back ache

TNF alpha blockers for severe AS

local steroid injections for temporary relief

114
Q

Define what Psoriatic Arthritis is. (PsA)

A

Inflammatory arthritis associated with Psoriasis but 10-15% of patients can have PsA without psoriasis.

115
Q

What are the clinical subgroups of PsA?

A
  1. Symmetrical polyarthritis (like RA)
  2. DIP joints
  3. asymmetrical oligoarthritis with dactylitis
  4. Spondylitis (spine involvement) with or without peripheral joint involvement
  5. Psoriatic arthritis mutilans
116
Q

What are the signs and symptoms of PsA?

A

Psoriasis

Nail involvement ( pitting, onycholysis)

Dactylitis

Enthesitis

Extra articular features ( eye disease)

117
Q

How do you diagnose PsA?

A

Bloods - inflammatory parameters raised and negative RF

X-Rays:

  1. Marginal erosions and “whiskering”
  2. “pencil-in-cup” deformity ( in severe cases)
  3. Osteolysis
  4. Enthesitis
118
Q

What is Reactive Arthritis?

A

A condition in which arthritis and other clinical manifestations occur as an autoimmune response to infection elsewhere in the body

119
Q

What are the signs and symptoms of reactive arthritis?

A
  1. Inflammatory synovitis
  2. Iritis ( ocular lesions)
  3. Keratoderma Blenorrhagica - brown raised plaques on soles and palms
  4. Circinate Balanitis - painless penile ulceration
  5. Mouth ulcers
  6. Enthesitis
  7. Reiter’s syndrome - urethritis, arthritis and conjunctivitis
  8. Fever, fatigue and malaise
120
Q

What are the most common infections associated with Reactive arthritis?

A

Urogenital e.g. chlamydia

Enterogenic - salmonella, shigella and Yersinia

121
Q

How do you diagnose Reactive arthritis?

A

ESR and CRP increase

culture stool if diarrhoea

Culture of blood and rine

HLA B27 positive

Joint fluid analysis - rules out infection

X-ray of affected joints

122
Q

How do you manage reactive arthritis?

A

No specific cure

splint affected joints acutely treat with NSAIDs or Local steroid injections

if symptoms > 6 months then use methotrexate

123
Q

What conditions are associated with Enteric arthropathy?

A
  1. IBD
  2. GI bypass
  3. Coeliac disease
  4. Whipple’s disease
124
Q

What are the signs and symptoms of Enteric arthropathy?

A

Arthritis in several joints (especially in the knees, ankles, elbows and wrists)

  1. GI - loose, stool with mucous and blood
  2. Weight loss, low grade fever
  3. Uveitis
  4. Pyoderma gangrenosum
  5. Enthesitis
  6. Oral ulcers
125
Q

How do you diagnose Enteric arthropathy?

A
  1. Upper and Lower GI endoscopy with biopsy showing Ulceration/ colitis
  2. Joint aspirate - no organisms or crystals
  3. Raised inflammatory markers - CRP, PV
  4. X-Ray/MRI shows sacroiliitis
  5. US shows synovitis
126
Q

What is Polymyositis and Dermatomyositis?

A

Rare conditions characterised by insidious onset of progressive symmetrical muscle weakness and autoimmune-mediated striated muscle inflammation

127
Q

What are the signs and symptoms of Dermatomyositis/Polymositis?

A

Muscle weakness

insidious onset, worsening over months

symmetrical, proximal muscles

often specific problems e.g. brushing hair and climbing stairs

Myalgia +/- arthragia

  1. Dermatosysositis - myositis plus skin signs
  2. Macular rash - shawl sign is +ve if over back and shoulders
  3. Lilac- purple rash on eyelids often with oedema
  4. Nailfold erythema

lungs - ILD and respiratory muscle weakness

Dysphagia

Myocarditis

maligancy in 15% of dermatomyositis and 9% in polymyositis

128
Q

How do you diagnose Dermatomyositis/Polymositis?

A

Muscle enzymes ( ALT,AST, LDH and CK) increase in plasma

muscle biopsy confirm diagnosis

Autoatibodies - anti Mi2, anti-Jo1 associated with acute onset and ILD

Confrontational ( direct testing of power) and Isotonic testing ( sit and then stand)

EMG ( electromyography) shows increases fibrillations and abnormal motor potentials

MRI shows muscle inflammation, oedema, fibrosis and calcification

129
Q

How do you manage Dermatomyositis/Polymositis?

A

Corticosteroids ( e.g. prednisolone)

Immunosuppression e.g. Azathioprine, Methotrexate, ciclosporin, IV immunoglobulin and Rituximab

130
Q

What are the clinical features of Polymyalgia rheumatica (PMR)?

A

Age >50yrs subacute onset

Ache in shoulder and hip girdle and morning stiffness

bilateral aching

fever

weight loss

anorexia

depression

muscle strength is normal

131
Q

What are the clincial features of Giant cell arteritis (GCA)?

A

Headache

Scalp tenderness

jaw claudication

Visual loss ( amaurosis fugax)

Tender, enlarged, non - pulsatile temporal ateries

132
Q

How do you diagnose PMR and GCA?

A

Raised ESR and CRP

AlkP raised in 30% of cases

Temporary artery biopsy

Temporal artery USS

133
Q

How do you manage PMR and GCA

A

PMR: Prednisolone - start at 15mg daily

GCA: Prednisolone - start at 40-60mg daily

gradual reduction in steroid dose over 18 months to 2 years

NSAIDs not effective

134
Q

What is Fibromyalgia?

A

Common cause of chronic MSK pain not associated with inflammation

commonest cause of MSK pain in women and 6:1 more likely in women too.

135
Q

What might occur before fibromyalgia?

A

Emotional or physical trauma

136
Q

What are the main risk factors of fibromyalgia?

A

Female sex

middle age

low household income

divorced

low educational status

137
Q

What are the main conditions associated with fibromyalgia?

A

Chronic fatigue syndrome

IBS

chronic headaches syndromes

138
Q

What are the signs and symptoms of Fibromyalgia?

A

Central

  1. Chronic headaches
  2. sleep disorders
  3. Dizziness
  4. Cognitive impairment
  5. memory impairment
  6. Anxiety
  7. Depression

Eyes

  1. Vision
  2. Problems

Systemic

  1. pain
  2. weight gain

Joint dysfunction of jaw

chest pain

Myofascial pain

  1. fatigue
  2. twitches

Morning stiffness in joints

problems with urinating

139
Q

How do you diagnose Fibromyalgia?

A

All normal

Diagnosis is clinical

ACR proposed diagnosis criteria:

  1. Patient experiences wide spread pain and associated symptoms
  2. Symptoms have been present at same level for >3 months
  3. No other condition otherwise explains the pain
140
Q

How do you manage Fibromyalgia

A
  1. Patient education
  2. Multi-disciplinary response
  3. Graded exercise programme
  4. cognitive behavioural therapy
  5. Anti- depressants e.g. SSRIs
  6. Analgesia
  7. Gabapentin and pregabalin
141
Q

Where does Hip pathology typically produce pain?

A

In the groin which may radiate to the knee

142
Q

What are the complications of a Total hip replacement?

A

Early local complications: Infection, dislocation, nerve injury of sciatic nerve, leg length discrepancy, DVT and PE.

Late local complications: Early loosening, late infection and late dislocation (due to component wear)

143
Q

What are the causes of Avascular necrosis ( AVN) in the Hip joint?

A

Primary/idiopathic

Secondary causes include:

Alcohol abuse

Steroids

Hyperlipidaemia

Thrombophilia

144
Q

What are the clinical features of AVN of the hip?

A

Groin pain

early cases may see only changes on MRI

Later cases show patchy sclerosis on weight bearing area of femoral head with a lytic zone underneath formed by granulation tissue from attempted repair.

Lytic zones form the ‘hanging rope sign’ on XRAY

The femoral head may then collapse with irregularity of the articular surface and subsequent secondary OA occurs.

145
Q

How do you manage AVN of the hip?

A

If condition detected early - pre collapse then drill holes can be used in the femoral neck and abnormal area of head to relieve pressure ( decompression)

Once collapse has occurred, then THR only option

146
Q

What is gluteal cuff syndrome?

A

Broad tendinous insertion of abductor muscles of the hip ( Mainly gluteus medius) is under strain and is affected by tendonitis and degeneration leading to tears.

147
Q

What are the signs and symptoms of gluteal cuff syndrome?

A

Patients have pain and tenderness in the region of the greater trochanter with pain on resisted abduction

148
Q

How do you manage Gluteal cuff syndrome

A

Analgesic and anti inflammatories

physiotherapies and steroid injections

No surgery! - no benefit

149
Q

When would you perform a Unicompartimental knee replacement (UKR)?

A

When the patient has isolated OA of the medial or lateral compartments of the knee as a less invasive surgery with less bone removal and preservation of the knee ligaments.

150
Q

What are the risks of surgery for knee replacements?

A

Infection

thrombosis

unexplained pain- higher in Total knee replacement than total hip replacement

151
Q

What are the main causes of meniscal tears of the knee?

A

Most common cause in sports injury for young patients e.g. squatting position

atraumatic spontaneous degenerate tears more likely to happen in older patient

152
Q

What are the clinical features of a meniscal tear of the knee?

A

Medial meniscal tears more likely than latera meniscal tears - medial meniscus more fixed and less mobile

Knee pain - on the tibial rotation localising the affected compartment (Steinmann’s test)

Effusion

Joint line tenderness

Acute Locked knee signifies displaced ‘bucket handle’ meniscal tear (15 degrees springy block to full extension). Also called knee locking

153
Q

How do you diagnose Meniscal tears?

A

Imaging :

MRI - gold standard

X RAY - used if associated fracture is suspected

McMurray’s test positive

Classification: many types of meniscal tears with differing patterns

  1. Longitudinal tears
  2. Radial tears
  3. Oblique tears
  4. Horizontal tears
  5. “bucket handle tear” - long longitudinal tear.
154
Q

What is a meniscus tear?

A

A tear of a meniscus is a rupturing of one or more of the fibrocartilage strips in the knee called menisci.

155
Q

What is a degenerate meniscal tear?

A

When the meniscus tears spontaneously/ with seemingly innocuous injury

occurs as the meniscus weakens with age

156
Q

What does degenerate meniscal tear suggets?

A

1st stage of Knee osteoarthritis

157
Q

How can you differentiate between acute and degenerate meniscal tears?

A

Degenerate tears are Steinmann’s negative and are likely to be associated with early symptoms and signs of OA

158
Q

How do you manage meniscal tears?

A

90% of meniscal tears are not suitable for repair

Depends on presentation of meniscal tear

  1. Locked Knee - urgent arthroscopic meniscal surgery indicated
  2. Acute Injury with Meniscal target (MRI) - Meniscal preservation may be appropriate or arthroscopic meniscal surgery
  3. Meniscal target (MRI) with signs and symptoms of tear -
    i. if symptoms >3 months than consider Non-urgent Arthroscopic Partial Meniscectomy
    ii. If symptoms <3 months than consider Optimal Non operative treatment and Re assess e.g. Phyisotherapy, steroid injection and analgesia
  4. Possible Meniscal target with signs and symptoms of tear - further non surgical treatment is first line e.g. physiotherapy, steroid injection and analgesia
  5. Advanced Structural OA and Meniscal tear ( Arthritic symptoms/signs only) :

NO arthroscopic meniscal surgery. Removal of meniscal tissue may increase stress on already worn surfaces.

Physiotherapy, Provide information, weight loss, steroid injection and analgesia

159
Q

What are the main causes of ACL rupture?

A

Sports injury e.g. Football, rugby and Skiing

160
Q

What are the clinical features of ACL rupture?

A

Main complaint is rotatory instability with giving way on turning

Knee pain

Swelling (haemarthrosis or effusion)

161
Q

How do you diagnose an ACL rupture

A

Tests:
Lachman test

Anterior drawer test

Pivot shift test - needs a relaxed patient and cause pain so only a specialist should do it

MRI

X RAY

162
Q

What is ‘rule of thirds’ in regards to ACL ruptures?

A

1/3 of patients compensate and are able to function after a ACL rupture

1/3 of patients avoid instability by avoiding certain activities after a rupture

1/3 of patients do not compensate and have frequent instability or can’t get back to high impact sport

older patients more likely to compensate

163
Q

How do you manage ACL rupture?

A

Physiotherapy to strengthen give procioceptive training to the quadriceps and hamstrings muscles may help compensation

Older patients are more likely to compensate or cope with ACL deificent knee

Primary repair not effective in 40% of patients with ACL rupture and end up with having a reconstruction

Surgery ( reconstruction)

Required for professional sportsmen or young adults who are keen on high impact sport

however: does not treat pain nor prevent arthritis

Involves tendon graft being passed through tibial and femoral tunnels at the usual location of the ACL in the knee and secured to the bone.

Intensive rehabilitation is required and may take up to a year to recover and play sports again

164
Q

What occurs in the PCL rupture?

A

Direct blow to the anterior tibia or hyperextension injury

causes include Motorbike accidents or Dashboard injury

165
Q

What are the clinical features of a PCL rupture?

A

Popliteal knee pain and Bruising

isolated PCL rupture rare - occurs with other injury normally

there is instability of the knee joint and it is giving when the tibia is pushed posteriorly

positive posterior drawer test

Patients complain about being unstable when walking down the stairs

166
Q

How do you manage a PCL rupture?

A

PCL reconstruction usually occurs for multiple ligament injured knee

only consider surgical reconstruction of PCL rupture of those with severe Laxity and recurrent instability with frequent hyperextension or feeling unstable descending stairs

Surgical reconstruction - cadaveric Achilles tendon allograft

167
Q

How do you grade Knee ligament injuries?

A

Grade 1: sprain - tear some fibres but macroscopic structure intact

Grade 2: Partial tear - some fascicles disrupted

Grade 3 - Complete tear

168
Q

Why is a MCL tear not necessarily bad?

A

Fairly forgiving knee ligament with healing expected in the majority of cases with little or no instability

169
Q

What are the clinical features of a MCL tear?

A

Laxity and pain on valgus stress

Tenderness over the origin or insertion of the MCL

170
Q

How do you manage MCL tears?

A

Physiotherapy, rarely requires surgery. Should recover properly ( even with complete tear) unless combined with an ACL or PCL rupture

Acute tears - hinged knee brace

chronic MCL instability - MCL tightening or reconstruction with tendon graft

171
Q

What are the clinical features of LCL ruptures?

A

common to occur with PCL or ACL injury

Hyperextension and varus gives rise to injury

Pain
tenderness

Injury to common peroneal nerve from excessive stretch is high

Popliteal artery injury is common

172
Q

How do you manage LCL ruptures?

A

Complete rupture needs urgent repair if early ( 2-3 weeks)

Later reconstruction is required ( hamstring or other tendon)

173
Q

What do complete knee dislocations cause?

A

Rupture of all four knee ligaments and have a high incidence of neurovascular injury

174
Q

What are the clinical features of a Knee dislocation?

A

knee Pain

out of place joint

Popliteal artery injury - tear, intimal tear or thrombosis

Nerve injury - common peroneal nerve

compartment syndrome - increased pressure within one of the body’s anatomical compartments results in insufficient blood supply to tissue within that space

175
Q

How do you manage Knee dislocation?

A

External fixation for temporary stabilsation

Regular checks on the circulation of the foot are mandatory due to risk of thrombosis

Distal circulation concerns - vascular surgery assessment with stenting or by pass may be required

compartment syndrome - requires reperfusion especially after prolonged ischaemia. Fasciotomies may be necessary

Multiple ligament reconstruction common

176
Q

Who are most likely to be affected by patellar dislocation?

A

females have higher incidence

Adolescents

ligamentous laxity (loose ligaments)

Valgus knee- characterized by hip adduction and hip internal rotation

torsional abnormalities

177
Q

What are the causes of Osteochondral and chondral injuries?

A

Impaction of the articular surfaces

Direct blow ( patellar dislocation can lead to these types of injuries)

178
Q

What are the clinical features of Osteochondral and chondral injuries?

A

Knee pain

effusion

179
Q

How do you diagnose Osteochondral and chondral injuries?

A

XRay

MRI

Arthroscopy

180
Q

How do you manage Osteochondral and chondral injuries?

A

Acute injuries with large osteochondral fragments should be fixed with pins

Non-weight bearing areas or have little bone attached should be removed arthroscopically

Fibrocartilage ( scar type hyaline cartilage) may fill in the defect in the surface of the knee

microfracture - Bare bone defects can have drilled or holes made to induce bleeding. this promotes fibrocartilage formation from stems cells differentiating into chondroblasts

181
Q

What does the extensor mechanism of knee consist of?

from most distal to most proximal

A

Tibial tuberosity

Patellar tendon

Patellar

quadriceps tendon

quadriceps muscles

182
Q

What causes extensor mechanism ruptures?

A

Rapid contractile force ( e.g. lifting a heavy weight, falling over or spontaneously in a severely in a degenerate tendon)

patellar tendon ruptures occur in a younger age group (<40)

Quadriceps tendon ruptures occur in older patients (>40)

183
Q

What are the risk factors of extensor mechanism ruptures?

A
  1. History of tendonitis
  2. Chronic steroid use
  3. Diabetes
  4. RA
  5. chronic renal failure
184
Q

How do you diagnose Extensor mechanism ruptures?

A

Straight leg raise to determine if the extensor mechanism is intact

Obvious palpable gap in the extensor mechanism

Xrays reveal a high Pt rupture or low lying patella

US used for obese patients if Gap is not obvious

185
Q

How do you manage Extensor mechanism ruptures?

A

Surgical:

  1. Tendon to tendon repair

or

  1. Reattachment of the tendon to the patella

steroid injections for tendonitis of the extensor mechanism of the knee MUST BE AVOIDED due to high risk of tendon rupture

186
Q

What is Patellofemoral dysfunction?

A

Describes disorders of the patellofemoral articulation in anterior knee pain

187
Q

What are the clinical features of patellofemoral dysfunction?

A

Chondromalacia patellae ( softening of the hyaline cartilage)

Anterior knee pain - worse down hill

lateral patellar compression syndrome

Grinding or clicking sensation at the front of the knee and stiffness after prolonged sitting

188
Q

What are the risk factors for patellofemoral dysfunction?

A
  1. females (particularly in adolescents) - wider hips
  2. Joint hypermobility
  3. Genu valgum (knock knee)
  4. femoral neck anteversion
189
Q

how do you manage Patellofemoral dysfunction?

A

90% of cases improve with physio - aims at rebalancing quadriceps muscles

Taping may alleviate symptoms

Surgery is a last resort - involve releasing a tight lateral retinaculum or tibia tubercle transfer to aid patellar tracking

190
Q

What causes patellar dislocation?

A

direct blow or sudden twist of the knee

191
Q

how do you diagnose Patellar dislocations?

A

Small opacification on X RAY suggest medial facet of the patella striking the lateral femoral condle

A lipo- haemarthrosis occurs with characteristic X ray appearance

192
Q

What are the causes of Ankle Osteoarthritis?

A

Idiopathic/primary

consequence of previous injury e.g. football players

193
Q

What might repeated dorsiflexion of the ankle cause?

A

Anterior damage with osteophyte formation

194
Q

What are the clinical features of the ankle osteoarthritis?

A

signs and symptoms of OA

195
Q

How do you manage Ankle OA?

A

Pain on dorsiflexion may be improved with removal of the anterior osteophytes (cheilectomy)

2 surgical options exist for significant pain from advanced ankle OA:

  1. Arthrodesis - is perhaps a more reliable option than ankle replacement
  2. Ankle replacement - may afford better functional outcome due to some preservation of motion. Issue is large force placed on relatively small bones
196
Q

What is Hallux Valgus?

A

Deformity of the great toe due to medial deviation of the 1st metatarsal and lateral deviation of the toe itself

197
Q

What are the risk factors of Hallux valgus?

A

More common in females 4:1

familial tendency

Incidence increases with age

commoner with Rheumatoid arthritis

Commoner with multiple sclerosis

Commoner with cerebral palsy

198
Q

What are the clinical features of Hallux valgus?

A

Painful due to bunion formation - joint incongruence and a widened forefoot may cause rubbing of the foot in an inflamed bursa over the medial 1st metatarsal head

Ulceration and skin breakdown

Hallux can override second toe in severe cases

199
Q

How do you diagnose Hallux Valgus?

A

X-Ray

200
Q

How do you manage Hallux valgus?

A

2 forms: operative and non operative

Operative:

Indications - failure of non op, pain, lesser toe deformities, Lifestyle limitation , overlapping, ulceration, functional limitation

many osteotomies required - realigns the bones and soft tissue procedure to tighten slack tissues and release tight tissues

Non operative: shoe modifications ( make wider or padding) spacer in the first web space to stop rubbing too.

201
Q

What is Hallux rigidus?

A

OA of the first MTPJ

202
Q

What are the causes of Hallux rigidus?

A

idiopathic or secondary due to osteochondral injury

203
Q

How do you manage Hallux rigidus?

A

Conservative treatment: wearing stiff soled shoe to limit motion at the MTPJ. A metal bar can be inserted into sole of shoe.

dorsal osteophytes removal via cheilectomy can also help

Arthrodesis is “gold standard” surgical treatment: Prevents women from wearing high heals.

can also have joint replacement

204
Q

What is Morton’s neuroma?

A

Degenerative fibrosis of digital nerve near it’s bifurcation. Irritated nerves become inflamed and swollen

205
Q

What are the clinical features of Morton’s neuroma?

A

Women more likely as they wear high heels

Burning pain tingling radiating into the affected toes

Third interspace nerve most commonly involved followed by the second

206
Q

How do you diagnose Morton’s neuroma?

A

Loss of sensation in the affected web space

Mulder’s click test

US for demonstrating a swollen nerve

207
Q

How do you manage Morton’s neuroma?

A

Conservative management: Metatarsal pad or offloading insole

Steroid injection can be used to relieve symptoms

Neuroma may be excised

208
Q

What is Osteomyelitis?

A

Infection of bone including compact and spongy bone as well as the bone marrow

209
Q

What is the pathophysiology of osteomyelitis?

A

infection causes enzymes from leucocytes cause osteolysis and pus forms

Pus impairs local blood flow making the infection very difficult to eradicate

Sequestrum ( dead fragment of bone) forms and breaks off preventing antibiotics alone from curing the infection

Involucrum ( new bone around the area of necrosis) forms.

Staph aureus can infect osteocytes intracellularly making infection additionally difficult for the system to reach

210
Q

What are the signs and symptoms of acute osteomyelitis?

A

Usually occurs in children and immunocompromised adults

Septic arthritis occurs

children can form Brodie’s abscess ( sub acute osteomyelitis)

Pain in affected bone

fever

211
Q

What are the signs and symptoms of chronic osteomyelitis?

A

Develops from an untreated acute osteomyelitis

May be associated with sequestrum and/or involucrum

Infection tends to be in the axial skelton ( spine or pelvis) for adults with haematoegenous spread from pulmonary or urinary infections or from disctitis

pain

212
Q

What are the causative organisms for osteomyelitis?

A

Newborns (<4 months)- S. aureus. Enterobacter sp., Group A and B strep

Children ( 4- 14) S. aureus, group A strep, Haemophilus influenzae and Enterobacter sp.

Adults - S.aureus and occasionally Enterobacter or streptococcus sp

Sickle cell anaemia patients - S.aureus the most common, salmonella is unique for sickle cell anaemia

213
Q

How do you manage osteomyelitis?

A

Acute - “best guess” antibiotics IV unless there is abscess formation in which then you should use surgical drainage

second line antibiotics if infection fails to resolve or surgery may be performed to gain samples for culture

chronic - antibiotics can be useful in supression. Surgery recommended to gain deep bone tissue cultures to removes any sequestrum and to excise any infected

poorly controlled diabetics, IV drug abusers and other immunocompromised patients are at particular risk of osteomyelitis of the spine. Lumbar spine is the commonest location.

High dose IV antibiotics after CT guided biopsy to obtain culture

214
Q

What nerve is mostly likely to be compressed at:

i. Carpal tunnel
ii. cubital tunnel

A

i. Median nerve

ii. ulnar nerve

215
Q

Which takes the slowest to heal after a fracture

humerus

Radius

Tibia

A

Tibia - takes 16 weeks

216
Q

Which bone has the higher rate of non-union due to retrograde blood supply and avascularity of the bone?

supracondylar fracture

waist of scaphoid fracture

Proximal humeral fractures?

A

waist of scaphoid fracture

217
Q

Which nerve is most at risk of being damaged by the anterior dislocation of the shoulder?

A

Axillary nerve

218
Q

Which nerve is most at risk being damaged by the colles (distal radial) fracture?

A

Median nerve

219
Q

Which nerve is most at risk being damaged by the humeral shaft fracture?

A

Radial nerve

220
Q

A metatarsal stress fracture can be quickly and easily ruled out by a prompt xray of the affected foot true or false?

A

False- may not demonstrate a fracture for around 3 weeks until resorption at the fracture ends occurs or callus begins to appear. Bone scan or MRI may be useful to confirm diagnosis

221
Q

What is Myositis Ossificans?

A

condition where heterotopic ossificiation (bone forming outside the skeleton) occurs in muscles usually after an injury

can form after muscle contusions ( dead leg), fractures (especially elbow) and dislocations ( especially hip dislocation)

222
Q

What is the impingement syndrome?

A

where the tendons of the rotator cuff ( predominantly the supraspinatus) are compressed in the tight subacromial space during movement producing pain.

223
Q

What are the clinical features of the impingement syndrome?

A

Painful arc - between 60 to 120 degrees of abduction. can be variable as an inflamed area of supraspinatus tendon passes through the subacromial space.

Pain radiates to the deltoid and upper arm

Tenderness may be felt below the lateral edge of the acromion

224
Q

What are the causes of the impingement syndrome?

A

Tendonitis subacromial bursitis

Acromioclavicular OA with inferior osteophyte

A hooked acromion rotator cuff tear

225
Q

How do you diagnose impingement syndrome?

A

Hawkins-Kennedy test (internally rotating the flexed shoulder) - recreates the patient’s pain

Cervical radiculopathy should be excluded from history and examination

Imaging - X ray, MRI and US

226
Q

How do you manage Impingement syndrome?

A

Conservative management: NSAIDs, Analgesics, physiotherapy and subacromial injection of steroid.

Subacromial decompression surgery to create more space for the tendon to pass through.

EITHER : Open procedure - incision large enough to visualise the subacromial space

or

Minimally invasive arthroscopic technique - small instruments and a keyhole camera are inserted into the subacromial space to perform the surgery

227
Q

What are the risk factors of rotator cuffs?

A

Athletes - throwing events

Manual workers (painters)

Occurs after a sudden jerk ( holding a rail on a bus which stops suddenly)

> 40 years of age with pain and weakness

20% of over 60s have asymptomatic cuff tears due to tendon degeneration

228
Q

What are the clinical features of the rotator cuff tears?

A

Supraspinatous muscle most commonly affected due to its superior location

dull achy pain which gradually increases

Pain present usually in all four tendons of the rotator cuff

tenderness over the shoulder around the glenohumeral joint and the AC joint

Patients tend to have difficulty sleeping on the affected side, reaching overhead e.g. to get something off a high shelf and pain on lifting

Typically have a painful arc with rotator cuff weakness

229
Q

How do you diagnose rotator cuff tears?

A

Imaging- MRI, US and XRay

Positive impingement signs from tests:
Hawkins-Kennedy test

Jobe’s test- also known as the relocation test and empty can test, is an orthopedic examination used to test stability of the shoulder.

Scarf test- scarf test is used to determine the integrity of the acromioclavicular joint

230
Q

How do you manage rotator cuff tears?

A

Surgery: Rotator cuff repair with subacromial decompression - improves/maintain strength and to prevent subsequent arthritis from chronic cuff deficiency.

Non- operative :
physiotherapy
subacromial injections may help with symptoms

231
Q

What is acute calcific tendonitis?

A

Results in the acute onset of severe shoulder pain and is characterised by calcium deposition in the supraspinatus tendon

Manage with subacromial steroid and local anaesthetic injection

Condition is self-limiting with pain easing as the calcification reabsorbs

232
Q

What are the two types of shoulder instability?

A

Traumatic instability

Atraumatic instability- patients with generalised ligamentous laxity ( idiopathic, Ehlers-Danlos, Marfan’s)

233
Q

What are the clinical features of bicep tendonitis?

A

Anterior shoulder pain with pain on resisted biceps contraction

Surgical division of the tendon with or without attachment to the proximal humerus may be required to relieve symptoms.

234
Q

What can cause referred shoulder pain?

A

neck problems

Angina pectoris

Diaphragmatic irritation

235
Q

What is Lateral epicondylitis ( tennis elbow)

A

condition where there is pain tenderness over the lateral epicondyle

236
Q

What are the clinical features of the lateral epicondylitis?

A

Painful and tender lateral epicondyle and pain on resisted middle finger and wrist extension

pain on resisted middle finger and wrist extension

can be a repetitive strain injury

237
Q

How do you diagnose Lateral epicondylitis?

A

US and MRI

NCS if there any nerve symptoms

Mill’s test is positive

238
Q

How do you manage Lateral Epicondylitis?

A

Usually self limting

Rest from activities that exacerbate pain

Physiotherapy

NSAIDs

Steroid injections

Local anaesthetic injections

Elbow clasp ( brace)

surgical release for refractory cases

239
Q

What is Medial epicondylitis (golfer’s elbow)

A

Condition caused by repeated strain or degeneration of the common flexor origin.

less common than lateral epicondylitis

Usually treated same way as lateral epicondylitis. However injection has risk of injury to the ulnar nerve

240
Q

What is the carpal tunnel syndrome?

A

condition involving the compression of the median nerve at the wrist as it competes for space along with 9 flexor tendons in the carpal tunnel

more common in women due to smaller wrist sizes

241
Q

What are the clinical features of the carpal tunnel syndrome

A

Aching pain in the hand and arm - especially at night

Paraesthesia in the thumb, index and middle fingers - relieved by dangling the hand over the edge of the bed and shaking it ( wake and shake)

may be sensory loss and weakness of abductor pollicis brevis

242
Q

what are the causes of the carpal tunnel syndrome?

A

Anything causing swelling or compression of the tunnel:
myxoedema

prolonged flexion

acromegaly

myeloma

local tumours

RA

amyloidosis

pregnancy

sarcoidosis

243
Q

How do you diagnose carpal tunnel syndrome?

A

confirm lesion site and severity

Phalen’s test- Maximal wrist flexion for 1 min

Tinel’s test - tapping of nerve at the wrist can induce tingling

244
Q

How do you manage carpal tunnel syndrome?

A

splinting

Local steroid injection

decompression surgery

245
Q

What is cubital tunnel syndrome?

A

Condition involving compression of the ulnar nerve at the elbow behind the medial epicondyle ( funny bone area)

246
Q

What are the clinical features of cubital tunnel syndrome?

A

Patients complain of paraesthesiae in the ulnar 1 1/2 fingers

Weakness of ulnar nerve innervated muscles may be present including the 1st dorsal interosseous (abduction index finger) and adductor pollicis

Tinel’s test usually positive

Froment’s test positive

247
Q

What are the two main causes for ulnar nerve compression at the cubital tunnel?

A

Tight band of fascia forming the roof of the tunnel ( osborne’s fascia)

Tightness at the intermuscular septum as the nerve passes through or between the two heads at the origin of the flexor carpi ulnaris

248
Q

how do you manage cubital tunnel syndrome?

A

rest and avoid pressure on nerve

if symptom continues then night time soft elbow splinting

if splinting fails or is chronic then decompression surgery can be used

249
Q

What is Dupuytren’s contracture?

A

profilerative connective tissue disorder where the specialised palmar fascia undergoes hyperplasia causing finger contractures at the MCP and PIP joints

250
Q

what is the pathophysiology of Dupuytren’s contracture

A

proliferation of myofibroblast cells and the production of the abnormal collagen ( type 3 instead of type 1).

skin of the hand may appear to be puckered.

Palpable nodules may be present

Ring and little fingers most likely affffected

251
Q

What are the risk factors of Dupuytren’s contracture?

A

Men more common

positive family history

smoking

alcohol

heavy manual labour

trauma

diabetes

Phenytoin

Peyronie’s diseases ( penis effecting disease) and Ledderhose disease also associated

252
Q

How do you manage Dupuytren’s contracture?

A

Collagenase injections

more than 30 degrees of contracture at PIP joint is an indication of surgery

either have:
fascietomy - removal of diseased tissue

Fasciotomy - removal of division of cords

253
Q

What is trigger finger?

A

Refers to tendonitis of a flexor tendon to a digit. Results in nodular enlargement of the affected tendon, usually distal to a fascial pulley over the metacarpal neck.

middle finger and ring finger most affected

254
Q

what are the clinical features of trigger finger?

A

Clicking sensation can be heard when fingers move

Pain in fingers

fingers may lock up in fexed position

patients may force finger to regain extension which can be painful

255
Q

How do you manage trigger finger?

A

steroid injection

surgery for persistent and recurrent cases

256
Q

What are the three stages of RA in the hands?

A
  1. synovitis and tenosynovitis - inflammation within the joints and the tendon sheath lead to swelling and pain in the affected structures
  2. Erosions of the joints - inflammatory pannus denudes the joints of articular cartilage
  3. Joint instability and tendon rupture - following the progressive destruction of the bony and soft tissue structures in the hand patients can progress to subluxation and chronic tenosynovitis predisposes to extensor tendon ruptures.
257
Q

What are ganglion cusys?

A

Common mucinous filled cysts found adjacent to a tendon or synovial joint.

258
Q

What are the clinical features of a ganglion cyst?

A

Common in the hand (DIP joint - mucous cyst)

common in the wrist ( volar wrist ganglion or dorsal wrist gangion)

can occur in the foot, ankle and knee ( baker’s cyst)

Localised pain/irritation

scars after removal may become tender

cysts are firm, smooth and rubbery

259
Q

How do you manage Ganglion cysts?

A

Needle aspiration ( watch out for radial artery if patient has a volar ganglion)

Surgical excision may be required if the swelling causes localised discomfort

DO NOT try to burst

recurrence rate very high if cyst is burst but wall of cyst is not removed

260
Q

What is the giant cell tumour of the tendon sheath?

A

second most common soft tissue swelling of the hand after ganglions.

usually found on the palmar surface around the PIP joints of index and middle fingers

261
Q

What are the clinical features of the giant cell tumour of the tendon sheath?

A

Brown

can cause pain

typically well circumscribed can be diffuse

can envelope the digital nerve/artery which can erode into bone

262
Q

What is the histology of giant cell tumour of the tendon sheath?

A

Contain multinucleate giant cells and haemosiderin (gives it a brown appearance)

263
Q

How do you manage giant cell tumour of the tendon sheath?

A

Excision to prevent local spread

recurrence can occur

264
Q

What is a pseudotumour?

A

Inflammatory granuloma produced in response to metal wear particles in the context of a joint replacement, which may be locally invasive but canont metastasise.

265
Q

The principal sign of adhesive capsulitis is what?

A

loss of external rotation of the shoulder

cant internally rotate or abduct too

266
Q

What are the risk factors of septic arthritis?

A

Pre-existing joint disease ( especially RA)

Diabetes

immunosuppression

chronic renal failure

prosthetic joints

joint surgery

IVDU

age >80 also more common in children than adults

267
Q

what are the signs and symptoms of septic arthritis?

A

Severely painful joints

signs of inflammation

tender joints

painful when moved

268
Q

what are the common causes of septic arthritis?

A

Staph aureus - most common cause in adults

streptococci - second most common cause

Haemophilus influenzae - now uncommon in areas where haemophilus vaccination is used. otherwise most common for kids

neisseria gonnohrea - rare in western europe

E.coli - found with elderly, IVDU and immunocompromised

269
Q

How do you diagnose septic arthritis?

A

urgent joint aspiration - frank pus then it is most likely septic arthritis

synovial fluid microscopy and culture

plain radiographs and crp may be normal

blood cultures

main differential diagnosis: crystal arthropathies

270
Q

How do you manage septic arthritis?

A

open washout used to decrease the bacterial load throughout the joint

antibiotics for gram positives e.g. flucloxacillin, vancomycin

271
Q

what is Slipped Upper Femoral Epiphysis (SUFE)?

ii. what is the main long term risk of SUFE?

A

when the head of the femur (thigh bone) slips off in a backwards direction, for reasons that are not known. It usually happens around puberty between the ages of 11 and 17 years and is more common in boys than girls

ii. Secondary OA

272
Q

which nerve is most at risk of damage from a middle of the humeras fracture?

A

radial

273
Q

adhesive capsulitis is more common in diabetics than non diabetics true or false?

A

true

274
Q

What is Takayasu’s arteritis?

A

is an inflammatory and stenotic disease of medium and large sized arteries

275
Q

what is the clinical presentation of Takayasu’s arteritis?

A

mainly in young women

Strong predilection for the aortic arch and its branches

malaise

fever

night sweats

arthralgia

anorexia

weight loss

absent pulse

arterial bruits

discrepancies in blood pressure

276
Q

what is the clinical presentation of multiple myeloma?

A

Bone pain - secondary to lytic lesions

confusion - secondary to hypercalcaemia

pancytopenia with macrocytosis

renal impairment

hyperclacaemia

ESR >100 mm/hour

277
Q

how do you diagnose multiple myeloma?

A

plain radiographs of all painful bony areas- to confirm lytic lesions

urinary bence- jones proteins

serum electrophoresis

278
Q

what are the five main subtypes of psoriatic arthritis?

A
  1. Rheumatoid arthritis- like : symmetrical polyarthropathy
  2. Asymmetrical arthritis: can affect any joint in the body: often a milder form
  3. distal arthritis: occurs in distal joints of fingers and toes; nail changes are common can lead to sausage shaped digits
  4. Spondylitis: inflammation of the neck and sacro-iliac joint- often HLA-B27 positive
  5. arthritis mulitans: severe destructive arthritis affecting small joints, erosisons develop quickly leading to deformity
279
Q

what is Felty’s syndrome?

A

RA

neutropenia

Splenomegaly

280
Q

which condition is a saddle nose deformity associated with?

A

GPA

281
Q

what is CREST syndrome?

A

Calcinosis - formation of calcium deposits in soft tissue

Raynaud syndrome - feel numb and cold in response to cold weather and stress

Oesophageal dysmotility

Sclerodactyly - hardening of the skin of the hand causing fingers to curl inward.

Telangiectasia

MSK (7 decks)

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